The host range of host-cell susceptibility to the leukosis-sarcoma viruses is dependent on specific interactions between genetically controlled properties of the viral envelope and the host-cell plasma membrane. The cell membrane "receptor" may act as an inherited alloantigen and be detectable by existing serological methods. One objective of this proposal is aimed at the serologic identification of erythrocyte alloantigens which may be associated with any of three different autosomal loci, each controlling susceptibility to a different viral subgroup--A, B, or C. A large colony of genetically variable chickens segregating for twelve systems or erythrocyte alloantigens and the three viral receptor loci will serve to supply appropriate recipients and donors to elicit anti-receptor hemagglutinins for one receptor and for as few erythrocyte alloantigens as possible. The already demonstrated association of R1 alloantigen with susceptibility to the B subgroup of viruses indicates that it should be possible to elicit allohemagglutinins for the A and C subgroups as well. Another primary objective is the investigation of the substructure of the alloantigen-determining portion of the B histocompatibility complex. The significance of this investigation rests on recent findings that certain B haplotypes either resist specific tumor formation or are very effective in regressing them. Recent evidence suggests that recombination within the B complex may be in the 1 to 2 per cent range which should allow for adequate recovery or recombinants under an efficient immunogenetic experimental design.